Today, postmenopausal women are at greater risk than younger women for cardiovascular diseases, due, in part, to increased hypertension. Factors likely to cause vascular dysfunction in both men and women are an age related elastin decrease, apparently due to increased activity of vascular elastases. This, coupled with calcium enhanced cholesterol deposition on elastin fibers and cross-linking brought about by the Maillard reaction stabilization of collagen fibers further increase age related hypertension. Together these factors may contribute greatly to blood pressure increases in both men and women but do not explain postmenopausal blood pressure rate increases. The long term goal of this pilot project is development of an independent research program intended to evaluate the effects of estrogen and other steroids on hypertension, arterial stiffening and other aspects of cardiovascular disease. If successful, areas of intended study will include examination both animal and human vessels recovered from surgery and tissue culture studies of vascular endothelia from rat, pig and human sources. Vascular viscoelasticity and structure will be examined in estrogen replete or depleted animals. The hypothesis this project will test is that estrogen depletion compromises the structure and function of elastic and conducting arteries in middle-age spontaneously hypertensive female rats. We intend to elucidate the mechanisms underlying this derangement. Estrogen induced alteration in arterial elastin and the high affinity 67 kDa elastin-laminin receptor, both of which are intimately associated with cardiovascular disease and neoplasia will be quantified biochemically. Maillard reaction products will be quantified biochemically. Presence of structural change in elastic and conductive arteries from estrogen replete and estrogen depleted animals will be examined using immunohistochemical techniques, histology as well as biochemical techniques. Estrogen loss is known to increase blood pressure in "normal" and spontaneously hypertensive female rats. Further, loss of this steroid is known to increase stiffening in great vessels. Already, exciting pharmaceuticals are known to reverse the effects of the Maillard reaction. These compounds or modifications of them may reduce arterial stiffening and improve future outcomes in hypertensive patients.